Hemodynamic Stability After Transitioning Between Endothelin Receptor Antagonists in Patients With Pulmonary Arterial Hypertension.
Abstract
BACKGROUND: Maintenance of a favourable hemodynamic profile is central to therapeutic success in pulmonary arterial hypertension (PAH).
There is little information about the safety of transitioning patients between oral therapies for PAH. Endothelin receptor
antagonists (ERAs) have been a therapeutic mainstay in PAH, providing benefit to many patients. Three ERAs, bosentan, sitaxsentan,
and ambrisentan have been approved for clinical use. Sitaxsentan was voluntarily withdrawn from the market in late 2010 resulting
in the need to quickly transition a large number of stable patients.
METHODS: We transitioned 30 clinically stable patients to either ambrisentan or bosentan. Patients underwent a right heart catheterization,
measurement of serum N-terminal pro-brain natriuretic peptide (NT-proBNP), and assessment of functional class before changing
ERA and again 4 months later. We present a retrospective analysis of those data.
RESULTS: Of the 30 patients transitioned (15 to ambrisentan, 15 to bosentan), 23 had complete hemodynamic data. No significant change
was observed in the groups in right atrial, mean pulmonary artery, and pulmonary artery wedge pressures, or in cardiac output,
pulmonary vascular resistance, or NT-proBNP levels. There was no change in World Health Organization functional class. Four
ambrisentan and 2 bosentan-treated patients reported fluid retention, and 3 bosentan-treated patients had elevation of hepatic
transaminases. Two of the patients had a right atrial pressure increase of ≥5 mm Hg, and 4 had pulmonary artery wedge pressure
increase of ≥5 mm Hg.
CONCLUSIONS: Transitioning between ERAs in stable PAH patients does not result in hemodynamic or clinical deterioration during the first
4 months posttransition. A minority of patients have developed increased cardiac filling pressures.
Links
Authors
Fox B, Langleben D, Hirsch AM, Schlesinger RD, Eisenberg MJ, Joyal D, Blenkhorn F, Lesenko L
Institution
Center for Pulmonary Vascular Disease, Jewish General Hospital and McGill University, Montreal, Québec, Canada.
Source
The Canadian journal of cardiology 29:6 2013 Jun pg 672-677Pub Type(s)
JOURNAL ARTICLELanguage
ENG
PubMed ID
22819360
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